The article discusses Programmed cell death 1 (PD-1) as a target for immune checkpoint inhibitor therapies that block its signaling to boost T-cell activity and its various functions across cell and cancer types. A study led by Brigham and Women’s Hospital identified PD-1 as an intrinsic receptor that promotes Merkel cell carcinoma (MCC) growth through mTOR signaling and mitochondrial reactive oxygen species production. The study found that inhibiting mTOR signaling and neutralizing mtROS suppressed MCC-PD-1-mediated tumor proliferation in mice. The authors suggest that targeting this tumor-intrinsic PD-1 signaling network could optimize immune checkpoint therapy regimens and improve MCC patient outcomes.
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Immune checkpoint inhibitor target found to promote skin cancer growth
